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PubMed1998

Definitions and terminology of compartment syndrome and Volkmann's ischemic contracture of the upper extremity.

Increased tissue pressure within the confines of a nondistensible anatomic compartment increases venous pressure, causes vascular compression, decreases the arteriovenous gradient, and results in a compartment syndrome. The decreased blood flow and hypoxia result in cellular damage of muscles, nerves, and vascular endothelium. Richard von Volkmann's legacy has taught us that a patient's overall status must be monitored to follow the systemic determinants of peripheral blood flow and oxygen transport. Limbs must also be monitored with vigilance. A high index of suspicion must always be present, and compartment pressures can be measured directly to aid in clinical decision making regarding the status of a compartment. The remaining articles in this issue describe and explore von Volkmann's syndrome using the terms and concepts introduced here.

Arm↗
PubMed1998

A historical review of compartment syndrome and Volkmann's ischemic contracture.

Compartment syndrome has been a recognized disease entity since the mid-nineteenth century. Extensive research and clinical observation have allowed for a better understanding of this uniquely complex disease process. Outstanding contributions by clinicians over the past century have provided the basis for our current perspective on its pathogenesis, diagnosis, and treatment. Although Volkmann's early reference to increased "pressure" as the cause of this syndrome was made over 100 years ago, today's modern concept of treatment to prevent contracture based on increased intracompartment pressure has evolved only through the combined efforts of various committed clinicians during the past century.

Compartment Syndromes↗
PubMed1987

Distribution of a neutral cardioplegic vehicle during the development of ischemic myocardial contracture.

During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37 degrees C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37 degrees C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (n = 9) or 90 mins (n = 9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67 +/- 1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33 +/- 0.18, the LV end diastolic pressure was 7.5 +/- 0.4 mmHg, and mean transmural myocardial adenosine triphosphate (ATP) was 16.4 +/- 1.1 microM/g DW. At the onset and throughout the first 45 mins of ischemia (n = 9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26 +/- 1.6 micron/g DW). After 75 mins of ischemia (n = 9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76 +/- 0.5 microM/g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82 +/- 2.0% and the subendocardial to subepicardial flow ratio was 1.75 +/- 0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure greater than 60 mmHg, n = 4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.

Adenosine Triphosphate↗